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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Molecular and cellular biochemistry 124 (1993), S. 43-49 
    ISSN: 1573-4919
    Keywords: IGF-1 ; IGFBP ; uterus ; mRNA expression
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract In previous studies, we have demonstrated that IGF-1 and IGF-1 receptor are expressed in rat uterus and that the expression is up-regulated by estrogen. The present study examines the expression and regulation of IGFBP-1 and IGFBP-3 in rat uterus throughout the estrous cycle. The stage of the estrous cycle in 16 mature female rats was determined by microscopic examination of daily prepared vaginal smears. Rat uteri were then used for RNA extraction. The results of the Northern blot analysis demonstrate that uterine cells express both IGFBP-1 and IGFBP-3 mRNA throughout the estrous cycle. When autoradiograms were quantitated by a densitometry, a significant reduction in expression of IGFBP-1 mRNA was found in uteri at stages of proestrous and estrous relative to that in diestrus. Although the level of IGFBP-3 mRNA varied in uteri throughout estrous cycle but this variation was not statistically significant. The lowest expression of IGFBP-1 (8.5% relative to diestrus, p〈0.05, n=4) and IGFBP-3 (71% relative to diestrus) was found in the uteri prepared from rats at the stage of proestrus, while the highest expression of IGFBP-1 and IGFBP-3 was observed in the uteri obtained from rats at the stage of diestrus and metestrus, respectively. Using anti-rabbit IGFBP-1 antibody raised against an oligo-synthetic IGFBP-1 peptide, immunohistochemical staining demonstrates the presence of IGFBP-1 in the luminal and stromal glandular epithelial cells. In summary, rat uterine cells express IGFBP-1 and IGFBP-3 mRNA and expression is regulated throughout the estrous cycle. A marked reduction in IGFBP-1 and IGFBP-3 during the proestrous stage of the estrous cycle may facilitate the biovailability of elevated IGF-1 to interact with IGF-1 receptor through a paracrine and/or autocrine mechanism.
    Type of Medium: Electronic Resource
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